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Although post-acute cognitive dysfunction and neuroimaging abnormalities have been reported after hospital discharge in patients recovered from COVID-19, little is known about persistent, long-term alterations in patients who did not require hospitalization. Therefore, we conducted a cross-sectional study of 87 consecutive, non-hospitalized recovered individuals, with a median of 54 days after the laboratory confirmation of COVID-19. We performed structured interviews, neurological examination, and 3T-MRI scans. The MRI study included white matter investigation with diffusion tensor images (DTI) and seed-based resting-state functional MRI (fMRI) connectivity analyses of the default mode network (DMN). In addition, we used validated instruments to examine fatigue, symptoms of anxiety and depression, somnolence, language, memory, and cognitive flexibility.Individuals self-reported a high frequency of headaches (40%) and memory difficulties (33%). The quantitative analyses confirmed symptoms of fatigue (68% of participants), excessive somnolence (35%), symptoms of anxiety (29%), impaired cognitive flexibility (40%) and language dysfunction (33%). In addition, we observed a correlation between DTI fractional anisotropy (FA) and abnormal attention and cognitive flexibility measured by the Trail Making Test part B. The resting-state fMRI study of the DMN showed an association between higher connectivity of the posterior cingulate cortex (PCC) and higher levels of fatigue and somnolence. While greater connectivity of the PCC with bilateral angular gyri was associated with higher fatigue levels, the elevated levels of somnolence correlated with higher connectivity between the PCC and both the left thalamus and putamen.

Background: Epilepsy is a risk factor for suicidal ideation (SI). SI still poorly investigated in caregivers of people with epilepsy (PWE). Aim: We aimed to analyze the prevalence and predictors of SI in adults PWE and caregivers. Methods: We analyzed 548 consecutive PWE (60% women; median age 41 [18-83]) and 191 caregivers (72% women; median age 47 [18-82]) followed at Outpatients’ epilepsy clinics from a tertiary center. We used “item nine” (item scores ≥1) of the BDI-II to determine the SI presence. The presence of symptoms of anxiety (with BAI) and depression (with BDI-II) was defined with scores ≥14 (for both PWE and caregivers). The presence of anti-seizure drugs (ASDs) adverse effects was defined with the “Liverpool Adverse Events Profile” score≥46. Epidemiological factors and anxiety were investigated as predictors of SI in caregivers and PWE (along with seizure frequency, epilepsy-type, and ASDs’ adverse events). Results: Depression was present in 41% of the PWE and 32% of the caregivers (p=0.04). Anxiety was observed in 37% of PWE and 33% of caregivers (p=0.32). The SI frequency was higher in PWE (19%) compared to the caregivers (11%; p=0.02). Logistic regression analyses were performed for both groups separately. For the PWE (model accounted for 17%-27%), the most significant predictors were anxiety (OR 4.4, p

COVID-19 patients may exhibit neuropsychiatric and neurological symptoms. We found that anxiety and cognitive impairment are manifested by 28-56% of SARS-CoV-2-infected individuals with mild respiratory symptoms and are associated with altered cerebral cortical thickness. Using an independent cohort, we found histopathological signs of brain damage in 25% of individuals who died of COVID-19. All of the affected brain tissues exhibited foci of SARS-CoV-2 infection and replication, particularly in astrocytes. Infection of neural stem cell-derived astrocytes changed energy metabolism, altered key proteins and metabolites used to fuel neurons and for biogenesis of neurotransmitters, and elicited a secretory phenotype that reduces neuronal viability. Our data support the model where SARS-CoV-2 reaches the brain, infects astrocytes and triggers neuropathological changes that contribute to the structural and functional alterations in the brain of COVID-19 patients.